I. Overview: Meige syndrome (Meige’s syndrome) is a segmental dystonia disorder. Some scholars also believe that Meige syndrome belongs to a kind of adult ADHD, which was first reported by French neurologist Meige in 1910. The main manifestations are bilateral blepharospasm, facial dystonia-like involuntary movements, also known as blepharospasm a mouthful of mandibular dystonia. Marsdan divided it into three types: (1) Blepharospasm type (BS): it presents with paroxysmal involuntary tightening-like spasmodic jerking or involuntary blinking of both eyelids. (2) Blepharospasm combined with oromandibular dystonia (BS-OMD): In addition to blepharospasm, the muscles of the mouth, lips, and jaws also contract spastically, showing pouting, lip contraction, mouth opening, tongue extension, and involuntary twitching of the corners of the mouth and facial muscles, and the patient has a strange expression. (3) OMD: Only spasmodic twitching of the mouth, lips and jaw muscles are present. Domestic scholars have added a type based on the above three types. (4) Other types: The above three types are combined with dystonia of the neck, trunk and limbs. Clinical manifestations: The disease usually starts in old age, mostly in 40-70 years old, mostly in women, with a male:female ratio of 1:2-3. It usually starts slowly, with a sense of irritation or discomfort in one or both eyes, shyness and increased frequency of blinking, and dry eyes, and later develops into blepharospasm. The symptoms worsen with fatigue, sunlight irritation, gaze, and stress, diminish when the mind is focused on something other than blepharospasm, and disappear during sleep. Most patients have paroxysmal blepharospasm as the first symptom. Blepharospasm is dominated by contraction of the orbicularis oculi muscle, with contraction of the frontal and nasal muscles centered between the eyebrows, manifested by an increased number of transients and lacrimation. Some patients start with eyelid spasms and gradually progress to the lower face, showing symmetrical irregular and hyperactive contractions of the oral and mandibular muscles, and tension of the mandibular muscles may prevent chewing, swallowing and speaking. Eyelid involvement: In mild cases, eye discomfort, dry eyes, photophobia, and increased transients may be manifested, and some cases may be misdiagnosed as “conjunctivitis”; in more severe cases, there may be episodes of difficulty in closing and opening the eyes, requiring the use of fingers to open the eyelids; in severe cases, functional blindness may result. Mouth-mandibular involvement: Involuntary mouth opening, mouth closing, pouting, lip retraction, cheek biting, tongue biting, and tooth bruxism. Neck muscle involvement: manifested as neck discomfort, sloping neck, head shaking, head tilting back, shrugging shoulders, etc. In severe cases, it is difficult to maintain normal head position. Other: Involvement of tongue muscle shows involuntary movements such as tongue retraction or tongue extension, tongue twisting, or tightness and stiffness of tongue root; involvement of pharynx may show pharyngeal discomfort, cough, slurred pronunciation and difficulty in swallowing; involvement of frontal muscle shows forehead tightness and frowning; involvement of hands and feet and limbs shows postural tremor, writing spasm, foot inversion and involuntary twitching; involvement of chest and abdomen may show local involuntary twitching with chest tightness and breath-holding. One of the characteristics of Meige syndrome is the dramatic reduction of symptoms seen when yawning, eating, coughing, singing, playing the piano, quizzing, playing the harmonica, or playing the mouth flute (Tricks phenomenon). Symptoms often stop developing within six months to two years, but there is great individual variability in the rate of progression, with some reaching their most severe level within a few weeks of onset and others showing a slow progression over 10 years. It has been reported that about 1/3 of patients suffering from Meige syndrome have psychiatric symptoms such as depression, but the mechanism is unknown. Diagnosis and differential diagnosis: 1. The diagnosis of the disease can be made mainly on the basis of the clinical features such as symmetrical and irregular contractions of the eyelid spasms and/or orofacial muscles, Tricks phenomenon, and disappearance during sleep. 2, Electrophysiological examination of the transient reflexes shows an increase in the frequency of transients, a significant increase in the amplitude of the R1 component (reflecting monosynaptic reflexes) and R2 component (reflecting polysynaptic reflexes), and a prolongation of the time frame of the electrically evoked corneal reflex. 3, PET-CT examination can see certain cortical or neural nuclei of the brain with reduced metabolism. 4, Trigeminal somatosensory evoked potential (TSEP) P19-N30 peak-to-peak amplitude is increased. Differential diagnosis: Meige syndrome should be differentiated from dry eye when early symptoms are atypical. The disease should also be differentiated from facial muscle spasm, tardive dyskinesia, orofacial dyskinesia, senile ptosis, functional perioral or eyelid hyperactivity, myasthenia gravis, tremor palsy, temporomandibular joint syndrome, and neurosis. The etiology and pathogenesis of primary Meige syndrome are still unclear. Most scholars believe that the pathogenesis of the disease may be related to damage to the basal ganglia of the brain, hypofunction of nigrostriatal γ-aminobutyric acidergic neurons leading to dopaminergic receptor hypersensitivity or dopamine transmitter imbalance, and imbalance of cholinergic action. The disease has also been reported to be associated with environmental factors that promote and genetic susceptibility resulting in decreased cortical inhibition; and close relationships have been reported with disorders of catecholamine metabolism, autoimmune dysfunction, familial genetic factors (a pure mutant gene 6-PTS viability residing in the CNS), and psychosomatic factors (55-80%). Secondary Meige syndrome has been reported to be associated with the use of certain medications, such as long-term use of psychosuppressive drugs, anti-convulsive paralytic drugs, anti-anxiety drugs, etc.; there are also studies showing that facial trauma, including dental surgery, can cause oromandibular dystonia, a phenomenon that is particularly pronounced in people prone to infection; and head trauma, nasopharyngeal radiation therapy, calcification of the basal ganglia or ischemic injury, etc. VI. Treatment The disease is currently treated symptomatically. Treatment methods mainly include oral medication, surgery, and local injection of botulinum toxin type A, etc. 1, conservative medical treatment Oral drugs include: (1) dopamine receptor antagonists, such as haloperidol, Tebrile, inosine, etc.; (2) γ-aminobutyric acid drugs, such as Jiajing Valium, sodium valproate, etc.; (3) anticholinergic drugs, such as Antan, etc.; (4) tranquilizers, such as diazepam, clonazepam, etc.; (5) antidepressants, such as amitriptyline, alpren, etc. (6) Anti-epileptic drugs: topiramate, levetiracetam, carbamazepine, etc. (2) Local injection of botulinum toxin type A. Botulinum toxin type A cannot restore the impaired motor activity in the cortical motor area and the ventral side of the premotor area, but can partially normalize the enhanced somatosensory activity caused by local facial muscle movements, indicating that botulinum toxin type A may have some significance in the recovery of brain function in this disease. the duration of action of botulinum toxin type A can last for several weeks to several months, and the main complication is local muscle paralysis. The drug is injected into the eyelids, perioral area and related areas of the face. About 30% of patients can have relief. In the early stage of the disease, due to the lack of understanding of the disease and the limitation of the treatment method, the surgical treatment method mainly used some destructive surgery, such as facial nerve avulsion, orbicularis oculi avulsion or excision, facial nerve orbicularis oculi branch destruction and stereotactic brain deep nucleus destruction, etc. These surgical methods are rarely used nowadays due to their poor efficacy and high chance of complications. These procedures are rarely used in clinical practice due to their ineffectiveness and high complication rate. The most advanced treatment method in the world is deep brain electrical stimulation, which is minimally invasive, reversible, adjustable and personalized, and is a safe and effective treatment with fewer side effects. The real point is that the current cost is more expensive. For patients with poor economic conditions, there is also the option of deep brain nucleus stereotactic disruption surgery. Our hospital is one of the first few hospitals in China to perform this type of surgery, with an efficiency rate of about 80-90% and an improvement rate of about 77-90%. However, the treatment of Meige syndrome is basically symptomatic, and there is a lack of specific methods for its eradication in domestic and foreign research.